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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

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Cardiac-specific overexpression of fibroblast growth factor-2 protects against myocardial dysfunction and infarction

Stacey L House¹, Craig Bolte, Ming Zhou

¹Department of Pharmacology and Cell Biophysics, University of Cincinnati, 231 Albert Sabin Way, ML 0575, Cincinnati, Ohio 45267, USA.

|December 6, 2003

Summary

Endogenous fibroblast growth factor-2 (FGF2) significantly protects the heart against ischemia-reperfusion injury. FGF2-deficient hearts showed impaired recovery, while FGF2-overexpressing hearts demonstrated enhanced function and reduced infarct size.

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A Modified Simple Method for Induction of Myocardial Infarction in Mice

A Modified Simple Method for Induction of Myocardial Infarction in Mice

Published on: December 3, 2021

Area of Science:

Cardiovascular Biology
Molecular Cardiology
Ischemia-Reperfusion Research

Background:

Preconditioning protects the heart from ischemic damage.
Fibroblast growth factor-2 (FGF2) is implicated in cardioprotection.
The specific role of FGF2 in ischemia-reperfusion injury is unclear due to multiple FGFs and ligand-receptor interactions.

Purpose of the Study:

To determine the role of endogenous fibroblast growth factor-2 (FGF2) in protecting the heart against ischemia-reperfusion (I/R) injury.
To investigate the effects of FGF2 deficiency and overexpression on cardiac function and infarct size following I/R.

Main Methods:

Utilized an ex vivo work-performing heart model with 60 minutes of low-flow ischemia and 120 minutes of reperfusion.
Compared FGF2-deficient (knockout) mice, cardiac-specific FGF2 transgenic (Tg) mice, and wild-type mice.
Assessed preischemic and postischemic contractile function, myocardial infarct size, and coronary flow.

Main Results:

FGF2 knockout hearts showed significantly reduced recovery (27%) compared to wild-type hearts (63%) after I/R (P<0.05).
FGF2 Tg hearts exhibited enhanced recovery (88%) and reduced infarct size (13% vs. 30% in WT, P<0.05).
No significant changes in coronary flow or capillary density were observed, indicating FGF2's protective effect is independent of perfusion changes.

Conclusions:

Endogenous FGF2 plays a critical role in the heart's protective response to ischemia-reperfusion injury.
FGF2 demonstrates significant cardioprotective effects, improving functional recovery and reducing infarct size.
These findings highlight FGF2 as a potential therapeutic target for mitigating I/R damage.